A strong willed person rarely develop syncope. We know weak hearted (Or is it weak brained ?) men and women may faint when the emotions swing unexpectedly .The commonest cause of syncope is neuro-cardiogenic syncope (NCS) . (Formerly called as vaso-vagal syncope VVS ). Few facts need to be emphasized here . There are many critical circuits and components to common syncope.

Trigger

Afferent

Center

Efferent

Fall /Near fall

Prompt recovery after the fall.

Trigger can be emotional or mechanical (Prolonged standing , dehydration , etc ) . It occurs generally in an emotionally charged environment with a high basal sympathetic tone .

Afferent for NCS is mostly sympathetic but it can be para- sympathetic also (Sensitive GI tract , Micturition etc )

* Many times a trigger and afferent pathway can overlap with each other.It is still unclear what exactly constitutes the afferent , since triggers can be either sympathetic or para- sympathetic . ( Pain, GI stimuli, vascular puncture etc) . Further , afferent can be be same as the trigger and reach the brain stem directly or touch the heart en route . ( Cardiac axis in classical NCS)

The center is in the medulla . Both vagal and sympathetic centers are involved with potential spill over on either side.

Final efferent pathway is the strong vagal surge resulting in bradycardia and peripheral vasodilatation , cerebral hypo-perfusion and the person usually falls .( Near fall or aborted NCS is also a common theme )

If stress increases the blood pressure , absence of stress will have to lower the blood pressure . If anxiety cause hypertension , depression is expected to cause hypo-tension.

These inferences may appear correct by logic . As is always in medicine , such logic works only partially ! ( We are told the Sadhus of Himalayas rarely record blood pressure beyond 100mmhg systolic !)

There are strong reasons to believe common syncope (NCS) is primarily related to the state of mind and the neural regulation. Dizziness , giddiness near syncope are closely related to psycho-somatic disorders. Strong willed men and women rarely develop syncope.Their vascular tone is well in control even in critical times .This fact has been well observed in the setting of traumatic and hemorrhagic shock in critical care units , where some hold their blood pressure well even in adverse circumstances and few sink without any fight .

Is psychogenic , situational , pain syncope same as NCS ?

Technically it may not be same. But all of them share at least 50 % 0f the circuits of NCS. .However there is no consensus to call psychogenic and pain syncope as types of NCS.

One critical aspect of the debate is , we do not know whether the cardiac axis is involved in these syncope or not. It is preferable to call these types of syncope as neural syncope (NS)

While in the classical NCS heart has a central role in generating hyper active sympathetic afferent from myocardial stretch receptors. In psychogenic and pain syncope cardiac stretch receptors are not much stimulated instead , the spillover occur directly from sympathetic to parasympathetic nucleus in medulla.

In pain induced syncope parasympathetic limb gets vigorously stimulated in isolation to cause a severe vaso-dilatation . But once the syncope sets in we often observe bradycardia and cardiac limb may get activated as well.

* Presence or absence of cardiac limb in NCS and NS is critical with reference to efficacy of beta blockers in NCS. The current guideline of NCS management( ESC 2010) is strongly biased against beta blocker (Class 3 -level A) which we feel is incorrect . Bulk of the patients with NCS respond well to long term beta blockers .

It doesn’t require great brains to realise vascular and neural system are intimately linked . We know today, NCS is primarily a neural phenomenon hence the mental status has a dominant control over the vascular system especially at times of stress .

The confusion between classical NCS and psychogenic / situational syncope can be largely avoided , if only we call these entities as simply neurogenic / neural syncope (NS ) ( Omitting the word cardiac is helpful , as cardiac axis is not vital here ? Non existent )

Clarity is still elusive in defining the trigger and afferent limb for the NCS , fortunately the final common efferent pathway that makes the patient fall is indisputably vagal ! . Medullary vagal nucleus though fires independently , also gets powerful central parasympathetic flow from cortical areas . Paradoxically , controlling sympathetic outflow (Anxiety ) is often an easier way to reduce parasympathetic flow. This is referred to as competitive , accentuated antagonism.

One can prevent recurrent syncope by vigorous mind control at times of extreme stress. This is confirmed indirectly , by the fact reassurance is the key to successful management in vast majority of patients with NCS .We learnt this simple fact after trying exotic methods like DDDR pacing and so on .

Final message

Power of the mind can never be under estimated even in cardio- vascular hemodynamics . When pathologically high, it can spike the blood pressure and break few vessels in brain , while if it is inappropriately low , may induce a syncope or result in persistent hypo-tension .

Let us learn to use our mind over body properly .Yogis do it style and live for 100 years !

Most cardiologists are familiar with “Circulation” . We know it is a top cardiology journal with highest impact factor. Few of us are aware of a journal called “Circulation research” ( I wonder why it is named like that , as if the regular circulation journal does not carry research stuff !)

It is one of the path breaking journals that regularly churn out state of the art , often mind boggling research stuff. Once in while we should get a feel of basic science research as it happens.

How else we are going to know an atrial cell is to be bio engineered shortly to behave like a SA node in patients with sinus node dysfunction. (Biological pacing )

This team from academic medical centre Amsterdam should be credited for publishing this gem of an article from a study involving the measly mice !

It deals elaborately about the embryonic basis of AV nodal disorders . Specifically it explains the genesis of WPW syndrome and how AV rings get muscularised .

(It is due to error in bio-genetic forces ,which affect the incorporation of AV nodal tissue in the fibrous skeleton .This results in ectopic junctional tissues appear any where along the AV ring . This is the basis of accessory AV pathway and clinical re-excitation.)

Final message

Once in a while we should develop the habit of reading tough journals like circulation research . After all , if a cardiologist is not reading these stuff who else . . . will ?

A middle aged man who owns a petty shop in a small town of south India came to us for stable angina .His RCA looked like this.

Normally if one coronary artery is obstructed the other comes to the rescue .It seems , this RCA do not trust it’s sibling LAD . See how it self supports its own territory .(The most fascinating and mysterious aspect of coronary circulation is the collateral circulation. LAD has big brother attitude . . . it hesitates to help others while RCA is more philanthropic , we know it sends prompt collateral to LAD whenever it is distressed !)

However , there is one advantage of such self-sustenance of RCA (Intra coronary/homo-collaterals ) . If the RCA has to live at the mercy of LAD it runs a risk of neglect at times of distant LAD ischemia as well !

Management

Single vessel disease , total occlusion , long segment lesion , still the PDA is protected and the vital postero- basal area of heart perfused well ! What to do ?

Scientific cardiologists would like to meddle this RCA with multi-pronged guide-wires and other weapons . Non -scientific cardiologists would send him home with medicines . This patient preferred the later ! In the process he saved a lakh , which I believe was meant for his daughter’s education . He profusely thanked me for not hijacking his hard earned money for frivolous reasons . I said he should thank his collaterals and not me , for getting his money back !

VPDs are the most common arrhythmia that confront us in cardiology clinics .While it can be a totally benign manifestation in some , it may signify a sinister condition in others. ECG is the easiest and surest way to identify VPD.However a shrewd echocardiographer can detect the VPDs while imaging the heart.It is often missed if one do not concentrate on the mitral valve motion.

One of the important hemodynamic side-effect of VPD is intermittent mitral regurgitation.

Effect of VPD on mitral valve opening .

By conventional thinking VPDs are expected to impact more on the mitral valve closure than it’s opening .In reality it has indirect influence on mitral valve opening as well. The retrograde conduction(VA conduction) of the VPD determine the timing of atrial contraction and hence the mitral valve opening. If the VPD gets blocked retrogradely within AV node , the normal sinus impulse will activate the atria in an antegrade fashion .Note , he atrial activity occur randomly when multiple VPDs occur.This makes the cardiac cycle too complex to assess especially the diastole. (In fact true physiological diastole may not occur here !)

If the mitral valve opening is interfered by a VPD (Early diastole is the favorite time for VPDs to appear ! ) .When it occurs the AML is suddenly pushed upon superiorly by the premature ventricular activity and hence resets the mechanical diastole. Please note electrical resetting of atrium is different from mechanical resetting.

It is also possible atria and ventricle contract simultaneously .This is the time , a cannon wave may occur inside LA .VPDs can result in pulmonary venous canons and may even elevate pulmonary venous pressure if this occurs repetitively .

Another possibility is , VPDs may not initiate a ventricular contraction at all .It may be simply be an electrical event. That’s why we changed the name of extra systole and premature contraction into just premature depolarisations.

Why is it important to know about M Mode motion of VPDs

Cardiologists continue to engage wide qrs tachycardias in the wrong side of their brain for many decades .The ECG debate about wide qrs tachycardia is expected to continue for generations . ! Few smart cardiologists would rapidly put the echo probe over the mitral valve and able to differentiate instantly a VT form SVT with fair degree of accuracy.

Detection of regular M shaped mitral AML will exclude a VT with a high degree of precision .(AV dissociation by echo )*

Even presence of trivial MR* (More often diastolic ) which occur irregularly will definitely indicate it is VT . SVT hemodynamically can not result in this MR is gives us evidence for AV dissociation

* No reference for these observed indices in our lab. (Class 1 Level C expert opinion( No one calls me as expert though ! )

What is the mechanism of VPD induced mitral regurgitation ?

It is well-known VPDs can cause mitral regurgitation .Not every VPD cause MR.

The timing is important .

It can be either systolic or diastolic MR .

If VPD occur in early diastole (After the T wave , the MR jet will collide with diastolic mitral flow. )

Paradoxical septal motion induced by VPDs can alter the pap muscle alignment transiently and result in MR

We dot not know how a LV apical VPD differ from RVOT VPD in the genesis of MR.

Logic would suggest RVOT VPDs are unlikely to result in MR as there is a time lag for the impulse to reach the LV base

What is the effect of VPD and Aortic valve opening ?

While every VPD promptly hits the mitral valve , aortic valve may or may not open with VPDs .Again timing and focus of VPD could be important.This is the reason during multiple VPDs only few open the aortic valve , that explains pulse deficit. (The so called missed beat )

Final message

Anterior mitral leaflet (AML) is the most mobile structure of the heart . Hence , it is not surprising to note sudden unexpected ventricular contraction will have maximum impact on this valve .

When VPDs occur in clusters or at random it has a complex effect on the mitral valve motion. This is responsible for palpitation , minimal mitral regurgitation and rarely trouble some pulmonary venous cannons and raise in pulmonary venous pressure .

Careful analysis of AML motion can give us useful clues to differentiate VT from SVT during wide qrs tachycardia

Though heart is primarily known as a mechanical organ , in reality it is a vital electrical organ as well . The entire mesh of electrical pathway from SA node to Purkinje fiber would easily cross a mile or two .Maintaining and protecting such a delicately woven network needs lots of electrical sense . It is not surprising to note , VT or VF can be induced virtually in every human heart if stimulated rapidly. Electrocution induced by VF is the typical example.Cardiac surgeons do it regularly before surgery .

So , inducible VT in the EP lab need to be defined in a strict manner .

VT must be triggered by a single stimuli (or two )

Multiple sites should not be stimulated(ideally single site , at most two )

It should be sustained.

Only mono-morphic VT has significance

Induced p0lymorphic VT has no clinical value.

Pharmacological stimulus such as isoprenaline can be used but reduces specificity.

*If a VT rapidly degenerate into VF it usually means a polymorphic VT while unstable irregular polymorphic VT could be same as VF )

How do you make sure what we induce in EP lab is same as the clinical VT ?

This is the most difficult task for electro -physiologists. In real life setting VT is often induced by ischemia hypoxia , local acidosis and electrolytic imbalance. However rarely mind this issue . In EP lab we induce it with artificial electrodes . Does it make sense to compare these two totally different set of triggers in real life and a virtual EP life . Ideally to confirm ischemic VT one has to induce ischemia in EP lab and look for VT . (Adenosine stress ? ) Further , only re -entrant VTs can be induced in EP lab by programmed stimulation . Automatic VTs can not be induced by stimulation .

The chances of inducing a VT in EP lab is directily proportional to the aggression of the electro physiologists and patience of the patient ! One can afford to use more aggressive protocols only if a clinical VT was recently the documented .

Electrical stress testing of heart

It may be tempting to refer induction of VT in EP lab as electrical stress testing for the heart. But fundamentally there is a difference between this and the conventional EST . Unlike exercise stress test the inducibility of VT highly unpredictable . It has far too many variables . (The surface area of contact , number , Intensity , site of stimuli , scar location , irritability of viable myocardium , inertness of scarred myocardium , and finally the cellular milieu etc )

Thoughts to ponder over Is it not “a fundamentally a wrong concept” to give importance to inducible VT ?

Why should we treat a clinically non relevant inducible VT ? We do not know yet whether inducible VT in other wise normal LV function has any long-term significance . Currently it makes no sense to intervene in VT if the LV function is good and the episodes are not clinical but only inducible.

Note: If there is severe LV dysfunction (EF < 30 % ) one can implant an ICD without an EP study . ( Of course to state more dramatically without even single documented VT !) MADIT 2

Final message .

A VT which is inducible in EP lab has no meaning , if the LV function is normal , while even a non-existent (potential )VT in the setting of severe LV dysfunction is vitally important !

Though we differentiate cardiac function into mechanical and electrical for academic purposes , it is astonishing to note how the heart is able to function as a single unit . We know today , the ultimate outcome of VT is not dictated by electrical status of the heart rather , the mechanical ability to with -stand sudden dis-organized ventricular contractions ( A ventricle with good contractile function has inherent capacity to extinguish most episodes of VT .(Myocytes with inbuilt biological ICDs ?)

It is a million dolor question why some VT remain as non- sustained while others rapidly degenerate into fast VT and VF thereafter

RVOT is the classical site of TOF murmur , but there is a rider . The murmur of TOF is inversely proportional to the degree of RVOT obstruction. (Contrary to VPS with intact IVS) .In severe TOF especially during spells the murmur attenuate dramatically and may disappear altogether. Hence a silent and quiet heart do not necessarily indicate a mild form of TOF .

Other possibilities also exist.

The VSD in TOF is large and do not restrict blood flow on either direction . Rarely restrictive VSD can generate a murmur across VSD.

Aortic flow is increased in all severe cases of TOF ( Highest in pulmonary atresia and VSD) Hence there is always a possibility of a soft systolic flow murmur across Aortic valve .

Other rare cause for systolic murmur is due to prolapse of tricuspid valve that occludes the VSD potentially causing TR and in the process may convert the VSD into restrictive type.

Aorta is connected to the left ventricle like a hose pipe.The energy generated within the LV myocardium is efficiently delivered to the root of the aorta. Mechano -coupling of LV with aorta is important means by which blood is is ejected into systemic circulation .

Even though aorta has mainly passive contraction and ( The wind- kessel effect) , the most powerful contractile force of aorta comes from the transfer of kinetic energy from left ventricle .

This helps us to measure the LV function simply by looking at the aortic wall motion.Since aorta is the final common exit for LV it effectively represents the global LV function . The ubiquitous errors during LV border tracing and it’s subsequent mathematical amplification can be avoided. Here is a patient with severe LV dysfunction whose aortic motion is depicted . We refer to this as ” rail roading” sign of Aorta which implies a critically dysfunctional LV . His EF was 23 % The aortic motion is esepcailly useful in categorizing severe LV dysfunction from moderate LV dysfunction (The sensitivity we feel is as high as sophisticated tissue motion Doppler protocols .Of course it may lack specificity !* as hardened aorta due to aging can confound the aortic motion )